Descriptions

Rainbow trout (Oncorhynchus mykiss) experience a variety of stressors in their natural environment as well as in aquaculture that can have negative effects on their physiology. The effects of physiological stress and endocrine disruption have been well described in fish. However, there is a scarcity of information on the effects of such stressors on the heart in fish. We examined gene expression in the rainbow trout heart in response to 17-ethinylestradiol (EE), the active ingredient in some oral contraceptives, as well as physiological stress. We also assessed contractile function, as a measure of cardiac performance, under conditions of increasing performance demands in sexually immature rainbow trout. In chapter 2, using qRT-PCR, we observed increased vitellogenin (vtg1) in the ventricle, along with, hepatic estrogen receptor (ERα) and vtg1 mRNA increased with EE exposure, confirming endocrine disruption in both tissues. Stress increased corticotropin-releasing factor receptor 1 (CRF-R1) and JunB in response to stress while nuclear protein 1 (nupr1) and glucocorticoid receptor (GCR2) expression increased only in the population with higher cortisol levels (>100 ng/ml) in response to stress. Interestingly, EE exposure did not affect stress induced gene expression and stress did not have an effect on EE induced gene expression in the heart of rainbow trout. This research highlights the fact that these stressors have the potential to have physiological impacts beyond the target tissues classically thought of for stress (i.e. HPI/A axis) or exposure to estrogenic compounds (i.e. HPG axis). In chapter 3, contractile force production was measured from ventricle strips exposed to increasing concentrations of Ca²⁺ or epinephrine to simulate conditions of increasing performance. Also, to determine the effects of physiological stress, ventricle strips were pre-treated with 100 ng/L cortisol prior to increasing Ca²⁺ or epinephrine. Ventricle strips from males had a greater contractile force production to increasing Ca²⁺ or epinephrine compared to females, at concentrations greater than 3.5 mM Ca²⁺ or 1 µM epinephrine. Exposure to cortisol did not have a direct effect on contractility, nor did it have an effect the contractile response to increasing exogenous Ca²⁺ in either sex. Interestingly, force production did not vary by sex in the cortisol pre-treated exposed to epinephrine, suggesting a sex-dependent response. My findings suggest that there are sex differences in the contractile function in rainbow trout and that these may be modified under conditions related to physiological stress. The rainbow trout is a genetically diverse species found across a variety of habitats. Our results highlight the variation in responses in in contractile function and gene expression in the heart by the different sexes, as well as variation within and among populations that allow rainbow trout to adapt and perform in the presence of stressors in the environment.